"感染负荷"目前被认为是动脉硬化新的危险因素。我们前期研究发现，金黄色葡萄球菌超抗原样蛋白-5(SSL5)可激活血小板，并释放大量的血小板微粒（PMs）；并且SSL5可加速动脉硬化病变的形成，但其机制尚不清楚。由于PMs具有促凝血和促炎症两方面的作用，因此推测SSL5作用下形成的PMs（SSL5-PMs）可能在加速动脉硬化病变形成中发挥重要作用。本项目拟采用流式细胞分析、ELISA、Western blot、RT-PCR等方法，研究SSL5-PMs对人单核细胞活化及细胞因子表达的影响；结合RNA干扰技术，深入研究CD40L/CD40信号通路的调节作用；体内实验研究SSL5-PMs加速apoE基因敲除小鼠动脉硬化的作用机制，以及SSL5中和性抗体对金黄色葡萄球菌感染所致PMs升高的防治效果。旨在阐明SSL5-PMs加速动脉硬化形成的作用和机制，并为动脉硬化病变的防治提供新的策略和依据。

Infectious burden is a new risk factor of arteriosclerosis. We have found that staphylococcus aureus superantigen-like protein-5 (SSL5) could activate platelets by binding to GPVI and GPIbα, and release a lot of platelet microparticles（PMs）. SSL5 also accelerated the formation of arteriosclerosis, but the exact mechanism is unclear. As PMs have both procoagulant and pro-inflammatory activities, the major assumption underlying this research is that SSL5-PMs(platelet microparticles from SSL5-activated platelets) may play a crucial role in the accelerated formation of arteriosclerosis. Using the following methods,such as flow cytometry analysis, ELISA, Western blot and RT-PCR,the monocytes' activation and cytokines expression from monocytes stimulated by SSL5-PMs will be assayed. Using RNA interference, further study will be performed on CD40L/CD40 signal transduction in the interaction between SSL5-PMs and monocytes. Animal experiments will be used for studying the acceleration role and the mechanisms of SSL5-PMs on atherosclerosis in apoE gene knockout mice. The neutralizing antibody of SSL5 (5E3) may prevent the PMs increase in Staphylococcus aureus infection. All studies above should be very important for clarifying the mechanism of SSL5-accelerated atherosclerotic lesions, and provide a novel strategy for the prevention of arteriosclerosis.